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Massive gains and improvements have been reported
by athletes and body builders using combination of Follistatin,
GHRP-6, ACE-031 and HMP.

These are available around the world but are
pricey as they really work well producing never seen before results.
Some body builders have reported 60% gain over 2 weeks using ACE-031
! Bundling Follistatin and GHRP-6 also produces results that no
steroid can duplicate ! Lean muscle gain beyond expectation.

This product has reported ridiculous permanent
growth of up to 60% in 2 weeks !

ACE-031 (Neuromuscular Disease treatment)

ACE-031 is a novel,
muscle-building agent that is being developed for the treatment of
patients with Duchenne Muscular Dystrophy with the goal of improving
strength and preserving physical function.

What is
ACE-031?

ACE-031 is an investigational protein therapeutic that builds muscle
and increases strength by inhibiting molecules that bind to and
signal through a cell surface receptor called Activin Receptor Type
IIB (ActRIIB). ACE-031 is a recombinant fusion protein that is
produced by joining a portion of the human ActRIIB receptor to a
portion of a human antibody. This creates a freely circulating,
decoy version of ActRIIB which removes proteins, such as GDF-8 (myostatin)
and other related molecules that limit the growth and strength of
muscle.

The
Role of ActRIIB Signaling and Muscle Growth

Muscle growth is regulated by proteins in the
TGF-β protein superfamily that serve as “on” or “off” switches for
muscle production. Several molecules including GDF-8 interact with
the ActRIIB receptor and send an “off” signal to stop muscle
production. In the absence of these “off” switch molecules that
signal through the ActRIIB receptor, muscle mass increases
dramatically.

Decreased ActRIIB Signaling Results in Muscle
Growth

In
nature, this effect has been observed in numerous species,
particularly in animals that have been bred for increased
musculature and strength. For example, Belgian Blue cattle lack the
gene for GDF-8, which is one of several molecules that activate the
ActRIIB receptor. A deficiency of this protein results in cattle
with tremendously developed musculature and strength. Similar
effects have been observed in other species, including rodents, dogs
and even humans.

Treatment with ACE-031 Builds Skeletal Muscle

Treatment with ACE-031 promotes muscle growth by inhibiting ActRIIB
signaling. ACE-031 binds to proteins that signal through the ActRIIB
receptor to limit muscle growth. When ACE-031 binds to these
proteins, it prevents them from interacting with the ActRIIB
receptor, thus allowing muscle to grow. Moreover, because ACE-031
prevents GDF-8 and other proteins that regulate muscle mass from
signaling through the ActRIIB receptor, its effects on lean muscle
exceed those of inhibitors of GDF-8 (myostatin) alone.

Non-Clinical
Results:

When
animals are treated with ACE-031, they experience growth in lean
muscle and are considerably stronger than their untreated
counterparts. This has been shown in several species, and in both
healthy animals and in animals with diseases associated with muscle
weakness and wasting.

Clinical Results:

Single Ascending Dose Phase 1 Study -Acceleron
completed a clinical study of ACE-031 (A031-01) in 48 healthy
postmenopausal women. These subjects received a single dose of
ACE-031 across a range of dose levels. For a description of the
study design,
click here. For the poster presentation of the study results
click here and
click here for the accompanying press release.

At higher doses, the effects of ACE-031 on
skeletal muscle were encouraging. After a single dose of ACE-031,
subjects developed roughly 1 kilogram (over 2 pounds) of muscle at 2
weeks. Moreover, ACE-031 altered biomarkers of fat metabolism
(increased adiponectin and decreased leptin) and bone formation and
resorption (increased BSAP and decreased CTX) at single doses of 1
and 3 mg/kg.

ACE-031 was
generally well-tolerated at all dose levels. No serious adverse
events were observed. The majority of adverse events were mild and
transient.

Multiple Ascending Dose
Phase 1 Study - A study in healthy
postmenopausal women (A031-02), evaluating multiple doses of
ACE-031, is currently ongoing. For more information on the study
design,
click here. Acceleron has presented preliminary results from
this study.
Click here for the poster presentation of these results and
click here for the accompanying press release. As this study is
not complete, final results are not yet available.

A031-02 randomized 60 subjects in 6 cohorts of
10 subjects each to receive ACE-031 or placebo (8:2) at dose levels
ranging from 0.1 to 3 mg/kg given by SC injection every two or four
weeks for a total of three or two doses, respectively, over a four
week period. Subjects were followed for 12 weeks after their last
dose. Although this safety study was not powered to assess
statistically significant changes in endpoints, multiple exploratory
statistical analyses were performed on the data.

Consistent with the findings of the single dose
study (A031-01), multiple doses of ACE-031 given to healthy
postmenopausal women were generally well tolerated and resulted in
rapid and sustained effects on muscle, bone and fat. The most common
adverse events were injection site reactions, headache and
nosebleeds. The majority of adverse events were mild and transient.
ACE-031 had a half-life of approximately 12 days, supportive of
dosing every 2-4 weeks.

Mean total body lean mass measured by DXA at day
36 increased by 5.2% from baseline in the group receiving ACE-031 at
1 mg/kg every 2 weeks. This was statistically significant compared
to the 0.4% increase in the placebo group (p=0.008) and was
sustained through day 57. Significant increases were also seen at
doses of 2 and 3 mg/kg every 4 weeks.

Mean thigh muscle
volume measured by MRI at day 36 increased by 4.1% from baseline in
the group receiving ACE-031 at 1 mg/kg every 2 weeks compared to
1.1% in the placebo group (p=0.012). Significant increases were also
seen at 2 mg/kg given every 4 weeks. No statistically significant
changes were observed in grip strength or functional tests in this
healthy volunteer safety study.

Total Whole
Body Lean Body Mass (DXA)
% Change (Mean +/- SE)

Thigh Muscle
Volume (MRI)
% Change (Mean +/- SE)

ACE-031
treatment led to a rapid and significant increase in a biomarker of
bone formation (BSAP) and decrease in a biomarker of bone
resorption (CTX) versus placebo.
Consistent with these effects, lumbar spine bone mineral density by
DXA increased up to 3.4% in the 2 mg/kg every 4 week group from
baseline to day 113, compared with a decrease of 1.5% in the placebo
group (p=0.001).

ACE-031
treatment also led to significantly altered biomarkers of fat
metabolism (increased adiponectin and decreased leptin) by day 8.
Total body fat mass measured by DXA decreased up to 8.2% from
baseline at day 113 in the 3 mg/kg every 4 week group compared with
an increase of 0.5% in the placebo group (p=0.024).

Acceleron is developing ACE-031 for the
treatment of patients with
neuromuscular diseases, such as Duchenne Muscular Dystrophy (DMD),
with the goal of improving strength and preserving physical
function. By affecting the muscle directly, ACE-031 may one day
offer hope to patients suffering from these debilitating diseases.

by Anthony Roberts - GHRP-6 is a
peptide in the growth factor family. It has strong effect
on the release of Growth Hormone (GH). Its main use is to
promote food intake by stimulating hunger and aid in energy
metabolism. It can be used in the treatment of GH
deficiency as well as cachexia, eating disorders and
obesity.

Background

Although still relatively new, peptides have
recently become popular as performance enhancing drugs.
GHRP-6 is currently available from a few research companies.

Action

The major side effect accompanied by the use
of GHRP-6 is a significant increase in appetite due to a
stimulating the release of Ghrelin, a peptide which is released
naturally in the lining of the stomach and increases hunger and
gastric emptying.

GHRP-6 causes stimulation of the anterior
pituitary gland which ultimately causes an increase in GH
release. Since GHRP-6 acts directly on the feedback loop
which signals the inhibition of GH release, when natural GH
secretion has been inhibited by long term synthetic use, GHRP-6
can be used to re-stimulate the natural production of GH.
GHRP-6 also affects the central nervous system, by protecting
neurons as well as increasing strength in a way very similar to
the way certain steroids in the
Dihydrotestosterone family do.

Benefits of increased Growth Hormone levels
through GHRP-6 stimulation include: an increase in
strength, muscle mass and body fat loss, rejuvenation and
strengthening of joints, connective tissue and bone mass.
Enhanced GH secretion also leads to the liver secreting more
IGF-1 (Insulin-Like Growth Factor 1), which is thought to be the
primary anabolic mechanism of action for Growth Hormone.

Technical Data

It has also been discovered that when GHRP-6
and insulin are used simultaneously, GH response to GHRP-6 is
increased (1). A recent study in normal mice showed significant
differences in body composition, muscle growth, glucose
metabolism, memory and cardiac function in the mice being
administered the GHRP-6 (2). There are still many
questions regarding this fairly new compound, scientists are
hoping with to gain a better clinical understanding of the
peptide through further research over the next few years.

User Notes

I used this stuff at a dose of 500-600 mcg/day
for awhile and found that the weight gain (mostly from an
increase in my appetite) was far too great. I gained a ton of
weight (on par with the most potent anabolics) but it wasn’t
pretty.

The effects on my joints were very beneficial
at that dose also, but I didn’t really find much of a drop off
when I lowered the dose to 100-200 mcg/day. In fact, I have a
sprinter friend who ran a personal best with a combination of
low dose GHRP-6 (100-150 mcg/day or so) and Anavar (20 mgs);
that wouldn’t be a huge deal but for the fact that this was done
while rehabilitating an injury!

On the other hand, even that low dose was too
much for a figure competitor I know, who gained far too much
weight from using GHRP-6 and ultimately had to discontinue using
it after only a couple weeks.

Although this stuff can have GH-like effects,
the weight increase makes any possible fat burning effects
almost unnoticeable. For a bulking cycle, and at the price, it’s
almost a must-have, if you’re looking to gain a ton of weight or
trying to rehab an injury.

HGH is a natural substance that is excreted by the pituitary
glands in the human body. As a person ages, the level of HGH
that their body produces decreases. However, Jintropin works
to raise levels of HGH back to a youth-like level, therefore
aiding in muscle growth, weight loss, and anti-aging.

Human growth hormone works by increasing the amount of IGF-1
that a person's liver excretes. IGF-1 increases cell count
and repairs damaged cells. Therefore, Jintropin works
indirectly to increase muscle density, decrease fat, and
slow the progression of aging by increasing the level of
IGF-1 produced in one's body.

Jintropin has been used successfully by body builders since
its release in China seven years ago. By using Jintropin,
one can increase the size of their pre-determined muscle
cells. After puberty, a person can only work to increase
size of their pre-determined muscle cells. Human growth
hormone raises the level of IGF-1 in a person's body back to
their pre-pubescent level, therefore allowing them to grow
new muscle cells.

Because Jintropin aids in muscle cell growth, it allows one
to develop an ideal muscle density. And, unlike steroids
that cause you to gain mostly water weight, human growth
hormone promotes only growth of lean muscle.

As a body building drug, Jintropin increases lean body mass,
shortens recovery time between workouts, and enhances
overall performance with less risk of detection than other
performance-enhancing drugs. Additionally, it strengthens
joints and ligaments and heals damaged tissue. Other body
building benefits of Jintropin include increased protein
synthesis abilities, an increase in the amount of insulin a
person can use effectively, and an increase in the amount of
anabolic steroids a person can use effectively.

Another beneficial effect of human growth hormone is
heightened energy levels and metabolism. Naturally produced
HGH is responsible for these effects in children, and, by
using Jintropin as an adult, you can feel the same energy as
you did in your youth. An increased metabolism means
increased fat loss. In fact, Jintropin can cause weight loss
even without exercise.

As an anti-ageing drug, human growth hormone is one of the
most effective products on the market. Aging, in fact, is
caused by the decreasing levels of HGH in one's body. As a
person ages, their body becomes lass and lass capable of
repairing their damaged cells. HGH heals the damaged cells
that are most responsible for aging. Jintropin promotes
smoother and less-wrinkled skin by repairing damaged skin
cells. It strengthens bones, even those that have been
damaged by osteoporosis. Additionally, it can repair damaged
brain cells and prevent memory loss.

Human growth hormone drugs are not new to the medical world.
Many major pharmaceutical companies have been manufacturing
HGH for years. However, it is only distributed by
prescription for children who suffer with growth
deficiencies. Additionally, purchasing HGH from a major
pharmaceutical company is very expensive.

However, body builders have been purchasing HGH on the black
market and using it successfully for years. Jintropin, the
most potent form of human growth hormone, is similar to
Humatrope -- an American brand of HGH that is prescribed by
physicians and is up to 4 times more expensive

Melanotan II is a synthetic version of melanocyte
stimulating hormone that was created, synthesized and
developed at The University of Arizona and the Arizona
Cancer Center. Melanotan II is a shortened, circular
version of the hormone peptide. Melanotan II has sunless
tanning capabilities and Libido Enhancing Effects.

HOW IT WORKS

Melanotan II, or MT-II as it is often referred to,
works by stimulating melanocytes to produce more Melanin
(Pigment) without the need for excessive UV exposure.
Most Users report a golden brown tan after 10mg to 20mg.

It also has the added side effect of increasing
libido, in both men and women.

The Department of Pharmacology, University of Arizona
College of Medicine published a study in 1998 that
involved ten men who suffered from psychogenic erectile
dysfunction. Their trial concluded that, “Melanotan-II
is a potent initiator of erections in men with
psychogenic erectile dysfunction and has manageable side
effects at a dose of 0.025 mg./kg.” [24]

A clinical study published in 2000 of 20 men with
psychogenic and organic erectile dysfunction conducted
at the Section of Urology of The University of Arizona
College of Medicine concluded, “that Melanotan II is a
potent initiator of penile erection in men with erectile
dysfunction.”

HOW IT IS USED

Typically MT-2 comes in 10mg vials of powder. This is
mixed with 2ml of water and then administered
subcutaneously with an insulin syringe. The typical dose
is .005mg/kg twice daily for the first 10 days,
thereafter 0.1 mg twice daily as a maintenance dose.

EG:

100kg person would use .5mg (10 units on insulin
syringe) twice daily for the first ten days, then .1mg
(2 units on insulin syringe) twice daily.

Scientists have developed a drug which could boost
female sexual desire. Tests in female rats are proving
promising, showing "significantly enhanced" sexual
behaviour.

Its developers believe it could be a more significant
development in the treatment of sexual dysfunction than
Viagra.

If human trials do prove successful, it could be on
the market within three years.

The drug, PT141, is being developed by researchers at
Concordia University, Montreal, Canada and Palatin
Technologies - the company which is developing it.

PT141 seems to encourage the female rats to actively
seek out the males for sex, which in turn heightens
their sexual arousal.

The drug, which comes in the form of a nasal spray,
has a virtually instantaneous effect.

The company is carrying out tests to see if the drug
benefits women who have normal sexual function.

A study involving men with erectile dysfunction is
also underway.

Experts in the UK stress research into the drug is
still at a very early stage, but say it is hopeful.
Currently, the only help available for women with sexual
dysfunction problems is psychological or sexual therapy.

Promising

PT141 is a copy of a hormone which has an effect on the
nervous system called alpha-melanocyte-stimulating
hormone.

It has been established that melanocyte-receptors in
the brain play a part in several behaviours including
sexual arousal.

So stimulating these receptors using PT141 may
stimulate sexual function.

A study of around 40 female rats showed a three- to
five-fold increase in solicitations in rats who were
given the drug compared to those which were not.

Jim Pfaus, professor of psychology at Concordia
University, is carrying out the research into PT141's
effects on female rats, and he told BBC News Online: "It
could be bigger than Viagra."

"There's nothing in the arsenal now to treat female
sexual dysfunction. That's one of the things that's
really promising about this drug.

"If you have a woman in a loving relationship, but
who just doesn't feel desire for sex, the question is
why. What goes on to inhibit that?"

He said it could be that there was an interruption in
the "chain of command" within the body which leads to
desiring sex.

Potential benefits

This drug may be able to "jump-start" the connection
that has failed, and the brain may re-learn the normal
arousal response.

He said: "It only affected solicitation. It didn't
affect the ability to copulate or the rate of
copulation."

Professor Pfaus accepts there is a long way to go
before the potential benefits can be confirmed, but he
said the history of research using male rats was
encouraging.

"We know of a good correlation between male rats and
male humans."

But he said it was not yet known if female rats and
humans were as similar.

Further research will look at whether repeated use of
the drug reduces its effectiveness.

Dr Annette Shadiack, director of biological research
for Palatin, said: "This has the potential to really
meet an unmet need.

She added that the research was aimed creating a
treatment which could "return a woman to her natural
function."

Lack of treatments

Dr Selim Cellek, a senior research fellow in sexual
dysfunction at the Wolfson Institute for Biomedical
Research at University College London, said of the PT141
research: "This is hopeful, it might work, but there
needs to be more research.

"It's acting on the brain, and we don't know much
about how female sexual behaviour is regulated in the
brain."

Dr Cellek said there was currently no drug treatment
available for female sexual dysfunction.

He added that the research into PT141 could help
understanding of female sexual arousal: "If you don't
know how the machine works, you can't fix it when it
doesn't."

IGF-1 is a peptide roughly the same structure and
size as insulin, or about 70 amino acids long. It
belongs to the peptide family of substances identified
as growth factors. It is a highly anabolic hormone
released in the liver as well as in peripheral tissues
such as skeletal muscle. In the body, IGF-1 is released
in response to the presence of Human Growth Hormone
(HGH). After intense resistance training, the body
experiences a surge in GH and IGF, and this is one way
that new muscle is built. Although GH is considered to
be highly anabolic, in actuality, IGF-1 is suspected to
be responsible for the primary anabolic activities of
GH.

IGF-1 builds new muscle tissue by promoting nitrogen
retention and protein synthesis. This causes the growth
of muscles through both hyperplasia (which is an
increase in number of muscle cells) and mitogenesis
(which is the actual growth of new muscle fibres).
Thus IGF-1 not only makes muscle fibres bigger, it makes
more of them as well!

IGF-1’s effects are not limited to building new muscle,
however. It has a potent effect on lipid (fat)
metabolism, and helps the body burn fat at a
significantly elevated rate. In addition, IGF-1 is both
a neuroprotector and neuropromotor, which improves
mental functions such as reflexes, memory, and learning
ability. IGF is also important for production of
connective tissue and insuring proper bone density.

Although IGF-1 is very potent at building muscle and
burning fat, the Lr3 IGF-1 version is roughly 2-3x as
powerful.

Lr3IGF-1 (Long R3 Insulin-like Growth Factor-I or
Long R3IGF-I) is an 83 amino acid analog of
human IGF-I actually comprising the complete human IGF-1
sequence but with the substitution of an Arg for the Glu
at position 3, as well as a 13 amino acid extension
peptide at the N-terminus. This makes Long R3IGF-I
significantly more potent (2-3x) than IGF-I in studies,
because it has a lower affinity to be rendered inactive
by IGF binding proteins, and consequently more potential
activity in the body.

Ipamorelin or NNC 26-0161, a polypeptide hormone, is
a growth hormone secretagogue and ghrelin mimetic and
analog developed by Novo Nordisk[3]. Ipamorelin belongs
to the most recent generation of GHRPs from the mid
1990s and causes significant release of growth hormone
by itself, due both to its suppression of somatostatin
(an antagonist to GHRH) and stimulation of release of GH
from the anterior pituitary, similar to GHRP-2 and
GHRP-6 which are compounds from the same class (growth
hormone releasing peptides).[1] The cells that produce
and release GH are known as somatotropes.[2] Like GHRP-2
and GHRP-6, ipamorelin does not have ghrelin’s lipogenic
properties. Like GHRP-2 and unlike GHRP-6 ipamorelin
never induces hunger in mammals. Ipamorelin acts
synergistically when applied during a native GHRH
(growth-hormone releasing hormone) pulse or when
coadministered with GHRH or a GHRH analog such as
Sermorelin or GRF 1-29 (growth releasing factor, aminos
1-29).[1] The synergy comes both due to the suppression
of somatostatin and the fact that ipamorelin increases
GH release per-somatotrope, while GHRH increases the
number of somatotropes releasing GH.[1,2]

There is also a secondary effect of neuronal excitation
in the hypothalamus caused by ipamorelin, which lasts
for approximately 3 hours after application, similar to
GHRP-2 and GHRP-6.

Ipamorelin has a unique property among the GHRP class of
peptides. That property is known as selectiveness. Raun
et al demonstrated the selectiveness of ipamorelin for
GH release only in a study:

The development and pharmacology of a new potent
growth hormone (GH) secretagogue, ipamorelin, is
described. Ipamorelin is a pentapeptide
(Aib-His-D-2-Nal-D-Phe-Lys-NH2), which displays high GH
releasing potency and efficacy in vitro and in vivo. As
an outcome of a major chemistry programme, ipamorelin
was identified within a series of compounds lacking the
central dipeptide Ala-Trp of growth hormone-releasing
peptide (GHRP)-1. In vitro, ipamorelin released GH from
primary rat pituitary cells with a potency and efficacy
similar to GHRP-6 (ECs) = 1.3+/-0.4nmol/l and Emax =
85+/-5% vs 2.2+/-0.3nmol/l and 100%). A pharmacological
profiling using GHRP and growth hormone-releasing
hormone (GHRH) antagonists clearly demonstrated that
ipamorelin, like GHRP-6, stimulates GH release via a
GHRP-like receptor. In pentobarbital anaesthetised rats,
ipamorelin released GH with a potency and efficacy
comparable to GHRP-6 (ED50 = 80+/-42nmol/kg and Emax =
1545+/-250ng GH/ml vs 115+/-36nmol/kg and 1167+/-120ng
GH/ml). In conscious swine, ipamorelin released GH with
an ED50 = 2.3+/-0.03 nmol/kg and an Emax = 65+/-0.2 ng
GH/ml plasma. Again, this was very similar to GHRP-6
(ED50 = 3.9+/-1.4 nmol/kg and Emax = 74+/-7ng GH/ml
plasma). GHRP-2 displayed higher potency but lower
efficacy (ED50 = 0.6 nmol/kg and Emax = 56+/-6 ng GH/ml
plasma). The specificity for GH release was studied in
swine. None of the GH secretagogues tested affected FSH,
LH, PRL or TSH plasma levels. Administration of both
GHRP-6 and GHRP-2 resulted in increased plasma levels of
ACTH and cortisol. Very surprisingly, ipamorelin did not
release ACTH or cortisol in levels significantly
different from those observed following GHRH
stimulation. This lack of effect on ACTH and cortisol
plasma levels was evident even at doses more than
200-fold higher than the ED50 for GH release. In
conclusion, ipamorelin is the first GHRP-receptor
agonist with a selectivity for GH release similar to
that displayed by GHRH. The specificity of ipamorelin
makes this compound a very interesting candidate for
future clinical development.[3]

Whereas GHRP-6 and GHRP-2 cause a release and
increase in cortisol and prolactin levels, ipamorelin
only selectively releases GH at any dose. Further, a
mega-dose of ipamorelin results in a concomitant
mega-release of GH (up to the entire amount present in
the pituitary), whereas GHRP-2 and GHRP-6 have limits of
approximately 1mcg/kg in humans for their maximal GH
release.[4,5]

CJC-1295 is a Long acting GHRH analog.
Growth-hormone-releasing hormone (GHRH), also known as
growth-hormone-releasing factor (GRF or GHRF) or
somatocrinin, is a 44-amino acid peptide hormone
produced in the hypothalamus by the arcuate nucleus.
GHRH stimulates growth hormone (GH) secretion from the
pituitary. GHRH is released in a pulsatile manner,
stimulating pulsatile release of GH respectively.

The active portion of this GRF or GHRH peptide can be
found as a 29 amino acid long peptide and is
appropriately named GHRH1-29. This pulsatile release of
various peptides is due to the negative feedback loop
that is part of the hGH axis and controls the amount of
hGH that your body produces to keep it in a homeostatic
environment. Despite the effectiveness of GHRH to
stimulate growth hormone release there are a number of
problems associated with using it in vivo. The most
noteworthy problem is the half life of the peptide,
which has been shown to be ~7 minutes using advanced
HPLC technologies that have proven to be very accurate.
The reason for this relatively short half life is due to
an enzyme called dipeptidylaminopeptidase IV (DPP-IV),
which has a high affinity for the amino acids Ala and
Pro and in the case of GHRH it cleaves the 1 and 2
positions that consist of Tyr-Ala, creating GHRH3-29, an
inactive form of the peptide. To prevent the problems
associated with natural GHRH, pharmaceutical companies
looked at new ways to increase the half life and
bioavailability of these smaller peptides with
technologies that work far different than other
technologies, such as PEGylation.
CJC-1295 is a synthetic modification of growth hormone
releasing factor (GRF) with D-Ala, Gln, Ala, and Leu
substitutions at positions 2, 8, 15, and 27
respectively. These substitutions create a much more
stable peptide with the substitution at position 2 to
prevent DPP-IV cleavage, position 8 to reduce asparagine
rearrangement or amide hydrolysis to aspartic acid,
position 15 to enhance bioactivity, and position 27 to
prevent methionine oxidation. By applying the Drug
Affinity Complex (DAC) technology to GRF, the peptide
selectively and covalently binds to circulating albumin
after subcutaneous (SC) administration, thus prolonging
its half-life. These substitutions are key in increasing
the overall half life of CJC-1295 but there lies an even
greater reason as to why the half life has been extended
from ~7 minutes to greater than 7 days! Bioconjugation
is a relatively newer technology that takes a reactive
group and attaches it to a peptide, which in turn reacts
with a nucleophilic (usually a partially negative
molecule) entity found in the blood to form a more
stable bond. Albumin, one of the most abundant
substances in the human body is chosen as the
nucelophile by this particular peptide thanks to a Cys34
thiol group that attracts it. By combining the
tetrasubstituted GHRH analogue with maleimodoproprionic
acid using a Lys linker, you create a GHRH peptide with
a high binding affinity for albumin. Once the CJC-1295
molecule has attached itself to albumin, it is given an
extended half life and bioavailability thanks to the
albumin preventing enzymatic degredation and kidney
excretion. In fact, bioconjugation is so effective that
there was less than 1% of CJC-1295 left unreacted in
vivo and over 90% was stabilized after subcutaneous
injection. This means that you get more of what you paid
for working for you. There was no DPP-IV degredation
observed on CJC-1295 in any of the various experiments
conducted.

Various experiments have been conducted to test the
effectiveness of CJC-1295 in vivo and the Journal of
Clinical Endocrinology & Metabolism has reported
dose-dependent increases in mean plasma GH
concentrations by 2-10 fold for more than 6 days and
increased IGF-1 concentrations 1.5-3 fold for 9-11 days
after a single injection!
(from the same study) Subcutaneous administration of
CJC-1295 resulted in sustained, dose-dependent increases
in GH and IGF-I levels in healthy adults and was safe
and relatively well tolerated, particularly at doses of
30 or 60 µg/kg. There was evidence of a cumulative
effect after multiple doses

Not only that but they proved the mean half life to be
5.8-8.1 days and after multiple doses showed mean IGF-1
levels remained above baseline for up to 28 days
following! No serious adverse reactions were reported in
any group.

Because of the long half-life and stability of the
CJC-1295 analog it may only need to be taken 1-2 times
per week. However research on GHRH knockout mice showed
that e/d injections where superior in increasing GH vs
every 48 or 72 hours. “GHRHKO animals receiving daily
doses of CJC-1295 exhibited normal body weight and
length. Mice treated every 48h and 72h reached higher
body weight and length than placebo-treated animals,
without full growth normalization.” These mice were
treated for 5 weeks.
However the flaw in this study appears to be that the
mice treated e/d were receiving a larger dose, so at
minimum cjc-1295 is dose dependent. Whether or not a
more frequent injection would prove to be beneficial is
yet to be determined.

MGF is a splice variant of the IGF
produced by a frame shift if the IGF
gene. MGF increase the muscle stem cell
count, so that more may fuse and become
part of adult muscle cells. This is a
process required for adult muscle cells
to continue growing.

Why PEGylate MGF?

MGF exhibits local effects in skeletal
muscle and without modification is not
systemic (can’t travel through the
body). The problem with synthetic MGF is
that it is introduced IM and is water
based so it goes into the blood stream.
MGF is not stable in the blood stream
for more than a matter of minutes.
Biologically produced MGF is made
locally and does not enter the
bloodstream and is short acting so
stability is not an issue. By PEGylating
the MGF we can make synthetic MGF
injected IM almost as efficient as local
produced MGF. Clinically proven Advanced
Pegylation, the technology of
polyethylene glycol (PEG) conjugation,
holds significant promise in maintaining
effective plasma concentrations of
systemically administered drugs. It does
this by surrounding part of the peptide
with a unique structure made of
polyethylene glycol, which can be
attached to a protein molecule. The
result of a correct PEGylation is simlar
to the protective mechanism of a turtle
shell. The polyethylene glycol groups
protect the peptide but don’t surround
it completely. The active sites of the
peptide are still free to do their
biological function. In this case the
shell is a negative charged shield
against positively charged compounds
that would affect the protein. This also
provides a nice steric chamber for the
peptide to reside in. So it’s a happy
turtle

Neurological research has shown that
utilizing PEGylated MGF resulted in a
longer more stable acting version of the
MGF peptide in serum/blood.

Bottom line

PEGylation can improve performance and
dosing convenience of peptides,
proteins, antibodies, oligonucleotides
and many small molecules by optimizing
pharmacokinetics, increasing
bioavailability, and decreasing
immunogenicity and dosing frequency.
PEGylation also can increase therapeutic
efficacy by enabling increased drug
concentration, improved biodistribution,
and longer dwell time at the site of
action. As a result, therapeutic drug
concentrations can be achieved with less
frequent dosing—a significant benefit to
patients who are taking injected drugs.

The PEG itself does not react in the
body and is very safe. PEG has been
approved by the US Food and Drug
Administration (FDA) as a base or
vehicle for use in foods and cosmetics
and in injectable, topical, rectal and
nasal pharmaceutical formulations. PEG
has demonstrated little toxicity, is
eliminated intact by the kidneys or in
the feces and lacks immunogenicity. The
risk associated with current PEGylated
drugs are due to the way the drug itself
acts not the PEG. MGF, as it is being
currently sold, is getting a bad rep
from people due to the fact they feel
that they are not seeing gains from it.
Many people believe that the use of MGF
in their cycles or protocols just flat
out won't work, however, this is far
from the truth.
More MGF information
Complete Overview of MGF or IGF-IEc

From its sequence, MGF is derived from
the IGF-I gene by alternative splicing
and has different 3' exons to the liver
or systemic type (IGF-IEa). It has a 49
base pair insert in the human, and a 52
base pair insert in rodents, within the
E domain of exon 5. This insert results
in a reading frame shift, with a
different carboxy (C) terminal sequence
to that of systemic IGF-IEa. MGF and the
other IGF isoforms have the same 5'
exons that encode the IGF-I ligand-binding
domain. Processing of pro-peptide yields
a mature peptide that is involved in
upregulating protein synthesis. However,
there is evidence that the carboxy-terminal
of the MGF peptide also acts as a
separate growth factor. This stimulates
division of mononucleated myoblasts or
satellite (stem) cells, thereby
increasing the number available for
local repair

During the early stage of skeletal
muscle development, myoblasts (muscle
stem cells) fuse to form syncytial
myotubes, which become innervated and
develop into muscle fibres. Thereafter,
mitotic proliferation of nuclei within
the muscle fibres ceases. However,
during postnatal (after development)
growth, additional nuclei are provided
by satellite cells (myoblast) fusing
with myotubules. Muscle damage-recovery
seems to have a similar cellular
mechanism, in that satellite cells
become activated and fuse with the
damaged muscle fibres (reviewed by
Goldring et al. 2002). This is also
pertinent to certain diseases such as
muscular dystrophy in which muscle
tissue is not maintained and which have
been associated with a deficiency in
active satellite (stem) cells (Megeney
et al. 1996; Seale & Rudnicki, 2000) and
in myogenic factors (Heslop et al.
2000). Skeletal muscle mass and
regenerative capacity have also been
shown to decline with age (Sadeh, 1988;
Carlson et al. 2001). The reduced
capacity to regenerate in older muscle
seems to be due to the decreased ability
to activate satellite cell proliferation
(Chakravarthy et al. 2000). The markedly
lower expression of MGF in older rat
muscles (Owino et al. 2001) and human
muscle (Hameed et al. 2003) in response
to mechanical overload has been
associated with the failure to activate
satellite cells, leading to age-related
muscle loss (Owino et al. 2001). Your
muscle cels can not grow once they have
reached a certain size unless they
obtain more nuclei from the myoblast.
MGF increases the myblast available to
donate their nuclei to the adult muscle
cell.
“MGF appears to have a dual action in
that, like the other IGF-I isoforms, it
upregulates protein synthesis as well as
activating satellite cells. However, the
latter role of MGF is probably more
important as most of the mature IGF-I
will be derived from IGF-IEa during the
second phase of repair. Nevertheless, it
has been shown that MGF is a potent
inducer of muscle hypertrophy in
experiments in which the cDNA of MGF was
inserted into a plasmid vector and
introduced by intramuscular injection.
This resulted in a 20 % increase in the
weight of the injected muscle within 2
weeks, and the analyses showed that this
was due to an increase in the size of
the muscle fibres (Goldspink, 2001).
Similar experiments by other groups have
also been carried out using a viral
construct containing the liver type of
IGF-I, which resulted in a 25 % increase
in muscle mass, but this took over 4
months to develop (Musaro et al. 2001).
Hence, the dual role MGF plays in
inducing satellite cell activation as
well as protein synthesis suggests it is
much more potent than the liver type or
IGF-IEa for inducing rapid hypertrophy.”

These results are based on actual
transplantation of the DNA coding for
the peptides. This is a permanent effect
and much more potent than IM injections
of the peptide itself. You will not see
a 20% increase in muscle mass through IM
injections as claimed above.